Sensory stimulation increases cortical expression of the fragile X mental retardation protein in vivo

• Published in: Brain research. Molecular brain research. Vol. 80; no. 1; pp. 17 - 25
• Main Authors: Todd, Peter K, Mack, Kenneth J
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 14.08.2000; Elsevier
• Subjects: Animals; Biological and medical sciences; Calcineurin; Calcineurin - metabolism; Chromosome fragility (bloom syndrome, ataxia telangiectasia, fanconi anemia, x-linked mental retardation...); Experience dependent plasticity; Fragile X Mental Retardation Protein; Fragile X syndrome; Fragile X Syndrome - metabolism; Intellectual Disability - metabolism; Kainic Acid; Male; Medical genetics; Medical sciences; Nerve Tissue Proteins - biosynthesis; Rats; Rats, Sprague-Dawley; RNA-Binding Proteins - biosynthesis; Seizures; Seizures - chemically induced; Sensory Thresholds - physiology; Somatosensory Cortex - drug effects; vibrissa; Disorders of the nervous system; Experience dependent plasticity; Fragile X mental retardation protein; Calcineurin; Fragile X syndrome; Kainic acid; Seizures; Chromosome fragility; Nervous system diseases; Cerebral cortex; Rat; Epilepsy; Rodentia; Central nervous system; Gene expression; Mental retardation; Protein; Vertebrata; Mammalia; Animal; Plasticity; Brain (vertebrata)
• ISSN: 0169-328X; 1872-6941
• DOI: 10.1016/S0169-328X(00)00098-X

Fragile X syndrome is a common cause of mental retardation that results from the absence of the fragile X mental retardation protein (FMRP), an RNA binding protein whose function remains unclear. Recent in vitro work has demonstrated that the protein is translated near the synapse in an activity dependent manner [33]. We therefore asked whether expression of FMRP might be altered by neuronal activity in vivo. Using immunoblots of different sub-cellular fractions of the rat somatosensory cortex, we show that the levels of FMRP increase significantly following unilateral whisker stimulation, a model of experience dependent plasticity. This increase is greatest between 2 and 8 h after the stimulus and is seen in both a synaptosomal fraction as well as a sub-cellular fraction enriched for polyribosomal complexes. In contrast, detectable levels of FMRP within the somatosensory cortex show either a decrease or no change after a kainic acid induced seizure compared to water treated controls. Our findings demonstrate that FMRP expression levels are modulated in vivo in response to neuronal activity and suggest a role for FMRP in activity dependent plasticity.